中華心理衛生協會

Purpose: Evidence from Stroop and the probe detection task has shown that anxious individuals reveal an attentional bias to threat, suggesting that anxiety may cause a deficiency in filtering out threatening stimuli. Recently, researchers using negative proming tasks have found the defect inhibition and cognitive avoidance processes in anxious individuals. However, research based on these two processes has produced inconsistent results; therefore we conducted this study. Negative priming effects, the increase in response time to targets previously encountered as distracters, were explained by attributing them to the attentional inhibitory mechanism that blocks access to distracter representations at prime display; they were also explained by the memory retrieval mechanism that retrieves the conflict tags at probe display. In this study we tried to confirm the defect inhibition hypothesis and assumed a vanished negative priming effect in anxious individuals. We also tried to see if there was a different threat-related negative priming that may differentiate between the inhibition and the retrieval process in these anxious individuals. Methods: Subjects included twenty two medication-free patients of obsessive-compulsive disorder (OCD) and twenty one medication-free patients of other anxiety disorders (OAD), as well as thirty matched healthy subjects without any psychiatric history. Each subject's anxiety level was evaluated by the use of the State-Trait Anxiety Inventory. The Flanker paradigm of the negative priming task was used. Subjects viewed prime-probe pairs of unfamiliar neutral and threatening faces and were required to decide whether target faces were the same or different while ignoring the distracting faces. The stimulus locations were fixed and the experimental variables were repetition (repeating and non-repeating) and stimulus valence (neutral and threatening). Subjects' button-push reaction times were recorded and analyzed by the use of the ANOVA statistical method. Results: In prime conditions, a significant interaction effect was found between prime conditions and groups as the result of a three by two ANOVA. Further comparison revealed that the OCD group had a significantly longer response time to the threatening distracting condition compared to the neutral distracting condition. In probe conditions, a significant interaction between probe conditions and groups was found. Healthy subjects showed significant negative priming effects toward both neutral and threatening stimuli. All patients' negative priming effects disappeared, except that OAD patients revealed a significant negative priming effect in threatening condition. Results remained the same after we controlled the variation in each subject's baseline reaction time by the use of the ANCOVA statistical method. The results of the scores of anxiety levels showed that both OCD and OAD groups had significantly higher levels of anxiety compared to the normal group. Conclusions: The defect inhibition hypothesis under anxiety was confirmed in this study. The results indicated that OCD patients might have a prevalent inhibition deficit toward distracting stimuli. On the other hand, OAD patients' responsive pattern might be explained by cognitive avoidance or an increased memory retrieval effect toward threatening distracting stimuli. We further hypothesized that anxiety may alter representations of distracters and result in a stronger threat-related retrieval process as well as a defect inhibition process. However, this hypothesis needs to be supported by future research. Relative neuropsychological pathology might be related to the dysfunctional amygdala, which processes the threat related stimuli and the facial stimuli as well. Some clinical meanings and applications were also discussed. More follow up research is necessary to differentiate the possible different roles played by the attention inhibition and the memory retrieval mechanisms in patients with anxiety disorders.